Evidence map›Paper›PMID 26912590›Full record

ArticleJournal of neurophysiology2016

Desensitization-resistant and -sensitive GPCR-mediated inhibition of GABA release occurs by Ca2+-dependent and -independent mechanisms at a hypothalamic synapse.

Reagan L Pennock, Shane T Hentges

Abstract read
In one paragraph

Article in Journal of neurophysiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
  5. GABAergic Inputs to POMC Neurons Originating from the Dorsomedial Hypothalamus Are Regulated by Energy State.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  6. Regulation of heterologously expressed 5-HTBritish journal of pharmacology · 2019
    Article
  7. Article
  8. Article
  9. The Relevance of AgRP Neuron-Derived GABA Inputs to POMC Neurons Differs for Spontaneous and Evoked Release.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Reagan L PennockDepartment of Biomedical Sciences, Colorado State University, Fort Collins, Colorado.
Shane T HentgesDepartment of Biomedical Sciences, Colorado State University, Fort Collins, Colorado hentgess@colostate.edu.

Funding

Opioid regulation of hypothalamic neuronsR01DA032562 · NIDA · COLORADO STATE UNIVERSITY · PI HENTGES, SHANE T · 2012 to 2016
$1.6M
Mechanisms by which MU Opioid Receptors Resist DesensitizationF31DA035586 · NIDA · COLORADO STATE UNIVERSITY · PI PENNOCK, REAGAN · 2014 to 2016
$102k
NIDA NIH HHS F31 DA035586NIDA NIH HHS R01 DA032562
6 · The paper itself

Abstract

Whereas the activation of Gαi/o-coupled receptors commonly results in postsynaptic responses that show acute desensitization, the presynaptic inhibition of transmitter release caused by many Gαi/o-coupled receptors is maintained during agonist exposure. However, an exception has been noted where GABAB receptor (GABABR)-mediated inhibition of inhibitory postsynaptic currents (IPSCs) recorded in mouse proopiomelanocortin (POMC) neurons exhibit acute desensitization in ∼25% of experiments. To determine whether differential effector coupling confers sensitivity to desensitization, voltage-clamp recordings were made from POMC neurons to compare the mechanism by which μ-opioid receptors (MORs) and GABABRs inhibit transmitter release. Neither MOR- nor GABABR-mediated inhibition of release relied on the activation of presynaptic K(+) channels. Both receptors maintained the ability to inhibit release in the absence of external Ca(2+) or in the presence of ionomycin-induced Ca(2+) influx, indicating that inhibition of release can occur through a Ca(2+)-independent mechanism. Replacing Ca(2+) with Sr(2+) to disrupt G-protein-mediated inhibition of release occurring directly at the release machinery did not alter MOR- or GABAB -mediated inhibition of IPSCs, suggesting that reductions in evoked release can occur through the inhibition of Ca(2+) channels. Additionally, both receptors inhibited evoked IPSCs in the presence of selective blockers of N- or P/Q-type Ca(2+) channels. Altogether, the results show that MORs and GABABRs can inhibit transmitter release through the inhibition of calcium influx and by direct actions at the release machinery. Furthermore, since both the desensitizing and nondesensitizing presynaptic receptors are similarly coupled, differential effector coupling is unlikely responsible for differential desensitization of the inhibition of release.

Indexed as

Inhibitory Postsynaptic PotentialsAnimalsCalciumCalcium ChannelsCalcium Signalinggamma-Aminobutyric AcidGTP-Binding Protein alpha Subunits, Gi-GoHypothalamusMiceMice, Inbred C57BLReceptors, GABA-BReceptors, Opioid, muSynapsesCalciumCalcium Channelsgamma-Aminobutyric AcidGTP-Binding Protein alpha Subunits, Gi-GoReceptors, GABA-BReceptors, Opioid, mucalciumGABAB receptormu opioid receptorPOMCstrontium

Identifiers

PMID26912590
PMCPMC4922459

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.